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Vol. 14, No. 23, pp. 3014-3023, December 1, 2000
1 Gene Expression Laboratory, 2 Howard Hughes
Medical Institute, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA;
3 Medical Toxicology, University of Colorado Health Sciences
Center, Denver, Colorado 80262, USA; 4 Department of
Veterinary Physiology and Pharmacology, Texas A&M University, College
Station, Texas 77843, USA; 5 Department of Developmental and
Cell Biology, University of California, Irvine, California 92697, USA
The cytochrome P450 (CYP) gene products such as CYP3A and CYP2B are
essential for the metabolism of steroid hormones and xenochemicals including prescription drugs. Nuclear receptor SXR/PXR (steroid and
xenobiotic receptor/pregnenolone X receptor) has been shown both
biochemically and genetically to activate CYP3A genes, while similar
studies have established constitutive androstane receptor (CAR) as a
CYP2B regulator. The response elements in these genes are also
distinct, furthering the concept of independent regulation. Unexpectedly, we found that SXR can regulate CYP2B, both in cultured cells and in transgenic mice via adaptive recognition of the
phenobarbital response element (PBRE). In a type of functional
symmetry, orphan receptor CAR was also found to activate CYP3A through
previously defined SXR/PXR response elements. These observations not
only provide a rational explanation for the activation of multiple CYP
gene classes by certain xenobiotics, but also reveal the existence of a
metabolic safety net that confers a second layer of protection to the
harmful effects of toxic compounds and at the same time increases the
propensity for drug-drug interactions.
[Key Words: CYP gene; nuclear receptor; SXR/PXR; CAR; metabolic safety]
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